Prostate cancer metastasis will claim the lives of over 30,000 Americans this year. Boring et al., Cancer Statistics 1991, 19. The mode of dissemination however, remains very poorly understood. An almost dogmatic view of metastasis holds that prostate cancer cells first spread through the prostatic capsule then into the lymphatics, and eventually hematogenously travel to bone. Byar et al., Cancer 1972, 30, 5; Winter, C. C., Surg. Gynecol. Obstet. 1957, 105, 136; Hilaris et al., Am. J. Roentgenol. 1974, 121, 832; McLaughlin et al., J. Urol. 1976, 115, 89; Jacobs, S. C., Urology 1983, 21, 337; Batson, O. V., Ann. Surg. 1940, 112, 138; Saitoh et al., Cancer 1984, 54, 3078-3084; Whitmore, W. F., Jr., Cancer 1973, 32, 1104. However, this model has been based on histopathologic studies which have significant limitations, and in actuality the sequence of metastatic events remain unknown. Solid tumor animal experiments suggest that only 0.01% of circulating cancer cells eventually create a single metastatic deposit. Fidler et al., Science 1982, 217, 998-1001; Liotta et al., Cancer Res. 1974, 34, 997; Schirrmacher, B., Adv. Cancer Res. 1985, 43, 1-32. Ostensibly, a single bone metastasis from human prostatic adenocarcinoma (PAC) could be generated by 10,000 circulating cancer cells (2 cells/1 ml blood). In the past, detection of such a low concentration of cells has been difficult or impossible. Recently, however, Wu et al. used keratin-19 (K-19) mRNA PCR to detect breast cancer micrometastasis in patient lymph nodes and bone marrow. Wu et al., Lab. Inv. 1990, 62, 109A. Miyomura et al., also reported the detection of minimal residual acute lymphoblastic leukemia by PCR in patients harboring the Philadelphia chromosome. Miyomura et al., Blood 1992, 79, 1366-1370.
A method of detecting the micrometastasis of prostate cancer would be greatly desirable.